The roles of microRNA in human cervical cancer.

MiR-1258 promotes the apoptosis of cervical cancer cells by regulating the E2F1/P53 signaling pathway.

Increasing evidence shows that microRNA (miR)‑381 is involved in the carcinogenesis and biologic progression of various types of cancer in humans. However, its potential biologic role and mechanism in pancreatic cancer remain to be elucidated. In the present study, the expression and functional role of miR‑381 in pancreatic cancer were investigated. It was found that miR‑381 was significantly downregulated in pancreatic cancer tissues and cell lines. The biological functions of miR‑381 were examined by measuring cell proliferation, migration, invasion and apoptosis in vitro and in vivo. The miR‑381 target gene and signaling pathway were identified by luciferase activity assay and western blot assay. In vitro experiments confirmed that the enforced expression of miR‑381 markedly suppressed cell proliferation, migration and invasion, and induced apoptosis in pancreatic cancer cells. By contrast, silencing the expression of miR‑381 had the opposite effect. In addition, miR‑381 inhibited xenograft tumor growth in vivo. Furthermore, ETS1 was identified as a direct target of miR‑381, and western blot analysis showed that miR‑381 negatively modulated the expression of ETS1. It was also demonstrated that miR‑381 serves a key role in pancreatic cancer cells through regulating the phosphoinositide 3‑kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) signaling pathway. In conclusion, the data obtained suggested that miR‑381 mediated cell proliferation, migration and invasion by targeting ETS1, partly through PI3K/AKT/mTOR signaling pathway. These results provide novel insights into understanding the potential effects and molecular mechanism of miR‑381 on pancreatic cancer. miR‑381 may serve as a novel potential marker for pancreatic cancer treatment in the future.

/pdf/mir-381-functions-as-a-tumor-suppressor-by-targeting-ets1-in-4n31gs9wty.pdf

miR‑381 functions as a tumor suppressor by targeting ETS1 in pancreatic cancer.

Background MiR-133a has been confirmed to be involved in the development of multiple cancers including non-small cell lung cancer (NSCLC). However, the precise molecular mechanism has not yet been fully elucidated. The purpose of this study was to investigate the functional role and underlying mechanism of miR-133a in the progression of NSCLC. Methods Quantitative real-time PCR (qRT-PCR) was performed to measure miR-133a and LASP1 expression in NSCLC tissues and cells. 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2H-tetrazolium bromide (MTT) assay was used to detect cell viability. The protein levels were measured by western blot. The tumor growth was measured by xenograft tumor formation assay. Results miR-133a was significantly decreased while LASP1 was increased in NSCLC tissues and cells compared with control groups. Moreover, overexpression of miR-133a suppressed cell viability, whereas miR-133a knockdown enhanced the viability of A549 cells. More importantly, LASP1 was verified as a direct target of miR-133a. Moreover, overexpression of miR-133a inhibited the epithelial-mesenchymal transition (EMT) and TGF-β/Smad3 pathways by regulating LASP1 in vitro. In addition, miR-133a mimic suppressed tumor growth by modulating the TGF-β/Smad3 pathway in vivo. Conclusions In conclusion, miR-133a acted as a tumor suppressor in lung cancer progression by regulating the LASP1 and TGF-β/Smad3 signaling pathway.

MiR-133a acts as a tumor suppressor in lung cancer progression by regulating the LASP1 and TGF-β/Smad3 signaling pathway.

To obtain a better understanding on the role of microRNAs in the progression of cervical cancer, a systematic review was performed to analyze cervical cancer microRNA studies. We provide an overview of the studies investigating microRNA expression in relation to cervical cancer (CC) progression, highlighting their common outcomes and target gene interactions according to the regulatory pathways. To achieve this, we systematically searched through PubMed MEDLINE, EMBASE, and Google Scholar for all articles between April 2010 and April 2020, in accordance with the PICO acronym (participants, interventions, comparisons, outcomes). From 27 published reports, totaling 1721 cases and 1361 noncancerous control tissue samples, 26 differentially expressed microRNAs (DEmiRNAs) were identified in different International Federation of Gynecology and Obstetrics (FIGO) stages of cervical cancer development. It was identified that some of the dysregulated microRNAs were associated with specific stages of cervical cancer development. The results indicated that DEmiRNAs in different stages of cervical cancer were functionally involved in several key hallmarks of cancer, such as evading growth suppressors, enabling replicative immortality, activation of invasion and metastasis, resisting cell death, and sustained proliferative signaling. These dysregulated microRNAs could play an important role in cervical cancer's development. Some of the stage-specific microRNAs can also be used as biomarkers for cancer classification and monitoring the progression of cervical cancer.

https://www.mdpi.com/2073-4409/10/3/668/pdf

A Systematic Review of MicroRNAs Involved in Cervical Cancer Progression.

An increasing number of studies have reported that microRNAs (miRNAs) are dysregulated in cervical cancer and serve critical roles in cervical oncogenesis and progression. Therefore, identifying the aberrantly expressed miRNAs implicated in the formation and progression of cervical cancer may provide key clues for the development of effective therapeutic targets in treating patients with this type of malignancy. In the present study, miRNA‑874 (miR‑874) was downregulated in cervical cancer tissues and cell lines, and this downregulation was associated with International Federation of Gynaecology and Obstetrics stage and lymph node metastasis. The restored expression of miR‑874 prohibited the proliferation, migration and invasion, but promoted the apoptosis of cervical cancer cells. In addition, E26 transformation specific‑1 (ETS1) was identified as the direct target of miR‑874 in cervical cancer. Inhibition of ETS1 served tumour‑suppressive roles similar to miR‑874 overexpression in cervical cancer cells. A series of rescue experiments revealed that restoring ETS1 expression abolished the tumour‑suppressing effects of miR‑874 in cervical cancer cells. Taken together, the results of the present study indicated that miR‑874 may serve as a tumour suppressor in cervical cancer by directly targeting ETS1. This function suggested that miR‑874 holds potential therapeutic applications in treating patients with this type of malignancy.

/pdf/microrna-874-is-downregulated-in-cervical-cancer-and-437tsu7cz2.pdf

MicroRNA‑874 is downregulated in cervical cancer and inhibits cancer progression by directly targeting ETS1

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MicroRNA‑874 is downregulated in cervical cancer and inhibits cancer progression by directly targeting ETS1